This is a multi-disciplined approach to the study of renal disease in childhood. Studies are in progress to define the nature of C3 nephritic factor and its mode of action; it has been determined that C3NeF is an oligoclonal IgG molecule. The control of C3 and C4 synthesis is being investigated in tissue culture and in cell-free systems in order to understand the metabolic basis of complement alterations in kidney disease. Lupus nephritis in WZB/W mice is being suppressed by tolerance induction to nucleotide bases. The effect of cortisone and tolerogen together in the amelioration of established murine lupus nephritis is under investigation. Ultrastructural studies of the zipper in renal glomeruli is being pursued with freeze fracture techniques. Experimental nephritis models are being examined in rats with regard to strain susceptibility and various modes of induction (i.e., Tamm Horsfall protein). Clinical studies of membranoproliferative and other glomerulitonephritides as well as minimal disease are being pursued.